Green S, Langberg H, Skovgaard D, Bulow J, Kjaer M
Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark.
J Physiol. 2000 Dec 15;529 Pt 3(Pt 3):849-61. doi: 10.1111/j.1469-7793.2000.00849.x.
Changes in the concentration of interstitial K+ surrounding skeletal muscle fibres ([K+]I) probably play some role in the regulation of cardiovascular adjustments to muscular activity, as well as in the aetiology of muscle pain and fatigue during high-intensity exercise. However, there is very little information on the response of [K+]I to exercise in human skeletal muscle. Five young healthy subjects performed plantar flexion exercise for four 5 min periods at increasing power outputs ( approximately 1-6 W) with 10 min intervening recovery periods, as well as for two 5 min periods with ischaemia at approximately 1 and approximately 3 W. Microdialysis probes were inserted into the gastrocnemius medialis muscle of the right leg to measure [K+]I, and K+ release from the plantar flexors during and after incremental exercise was calculated from plasma flow and arterial-venous differences for K+. Calf muscle pain was assessed using a visual analogue scale. On average, [K+]I was 4.4 mmol l(-1) at rest and increased during minutes 3-5 of incremental exercise by approximately 1-7 mmol l(-1) as a positive function of power output. K+ release also increased as a function of exercise intensity, although there was a progressive increase by approximately 1-6 mmol l-1 in the [K+] gradient between the interstitium and arterial-venous plasma. [K+]I was lower during ischaemic exercise than control exercise. In contrast to this effect of ischaemia on [K+]I, muscle pain was relatively higher during ischaemic exercise, which demonstrates that factors other than changes in [K+]I are responsible for ischaemic muscle pain. In conclusion, this study has demonstrated that during 5 min of dynamic exercise, [K+]I increases during the later period of exercise as a positive function of exercise intensity, ischaemia reduces [K+]I during rest and exercise, and the increase in [K+]I is not responsible for muscle pain during ischaemic exercise.
骨骼肌纤维周围间质钾离子浓度（[K⁺]I）的变化可能在心血管系统对肌肉活动的调节中发挥一定作用，同时也与高强度运动时肌肉疼痛和疲劳的病因有关。然而，关于人体骨骼肌中[K⁺]I对运动的反应的信息非常少。五名年轻健康受试者以逐渐增加的功率输出（约1 - 6瓦）进行了四个5分钟的跖屈运动，中间间隔10分钟的恢复期，还进行了两个5分钟的约1瓦和约3瓦的缺血运动。将微透析探针插入右腿的腓肠肌以测量[K⁺]I，并根据血浆流量和钾离子的动静脉差异计算递增运动期间及之后跖屈肌的钾离子释放量。使用视觉模拟量表评估小腿肌肉疼痛。平均而言，静息时[K⁺]I为4.4 mmol·l⁻¹，在递增运动的第3 - 5分钟期间增加约1 - 7 mmol·l⁻¹，呈功率输出的正函数关系。钾离子释放也随运动强度增加，尽管间质与动静脉血浆之间的[K⁺]梯度逐渐增加约1 - 6 mmol·l⁻¹。缺血运动期间的[K⁺]I低于对照运动。与缺血对[K⁺]I的这种影响相反，缺血运动期间肌肉疼痛相对较高，这表明除[K⁺]I变化之外的因素是缺血性肌肉疼痛的原因。总之，本研究表明，在5分钟的动态运动期间，[K⁺]I在运动后期随运动强度增加而增加，缺血在休息和运动期间降低[K⁺]I，并且[K⁺]I的增加不是缺血运动期间肌肉疼痛的原因。
